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1 recombination with a concomitant increase in sister chromatid exchange.
2 rmal replication intermediates and increased sister chromatid exchange.
3 within the repeats, facilitating slippage or sister chromatid exchange.
4 r maximal induction of replication-dependent sister chromatid exchange.
5 chromosomal aberrations and 3-fold elevated sister chromatid exchange.
6 patterns suggest mechanisms such as unequal sister chromatid exchange.
7 acilitate FA pathway activation and suppress sister chromatid exchange.
8 to an increase in the incidence of telomere sister chromatid exchange.
9 unctional BLM show 10-fold elevated rates of sister chromatid exchange.
10 synthesis and caused a 3-4-fold increase in sister chromatid exchange.
11 relatively normal XRCC1 levels but elevated sister chromatid exchange.
12 erence in HeLa cells leads to an increase in sister chromatid exchange.
13 gene conversion but maintain proficiency in sister chromatid exchange.
14 toxicant as well as an effective inducer of sister-chromatid exchange.
15 t functions in a protein complex to suppress sister-chromatid exchange.
16 Bloom's syndrome is an elevated frequency of sister chromatid exchanges.
17 DNA damage signaling, telomere fragility and sister chromatid exchanges.
18 ative capacity and an increased frequency of sister chromatid exchanges.
19 itro induced enhanced chromosomal breaks and sister chromatid exchanges.
20 elayed and reduced RAD51 response, and fewer sister chromatid exchanges.
21 This leads to an increase in sister chromatid exchanges.
22 A damage, and displayed elevated spontaneous sister chromatid exchanges.
23 the potential for loss of heterozygosity and sister-chromatid exchanges.
24 on in response to DNA damage, and suppresses sister-chromatid exchanges.
25 e of genome stability and the suppression of sister-chromatid exchanges.
28 recombination repair, we observed extensive sister chromatid exchanges after treatment with tirapaza
29 e fibroblasts displayed an increased rate of sister chromatid exchange and a high frequency of sponta
30 n cells results in an increased frequency of sister chromatid exchange and DNA damage sensitivity aft
34 ing membrane signaling, and the induction of sister chromatid exchange and HPRT mutations by very low
35 ely to be intact as basal and damage induced sister chromatid exchange and immunoglobulin gene conver
36 hyper-recombination manifested as excessive sister chromatid exchange and loss of heterozygosity.
38 re partially defective in the suppression of sister chromatid exchange and resistance to camptothecin
40 We conclude that ORD activity suppresses sister chromatid exchange and stimulates inter-homologue
41 n relieved the cells with the suppression of sister chromatid exchange and therefore led to a hyper-r
42 ase activity to suppress spontaneous unequal sister chromatid exchanges and DNA double-strand break-i
43 c mitotic recombination, a high frequency of sister chromatid exchanges and double strand DNA breaks,
44 telomeres, manifested as increased telomere sister chromatid exchanges and formation of telomere cir
45 ous recombination (HR), exhibiting decreased sister chromatid exchanges and HR-dependent repair as de
46 notype manifests as an elevated frequency of sister chromatid exchanges and interhomologue recombinat
47 ected into BS cells reduces the frequency of sister chromatid exchanges and restores BLM in the nucle
48 ary Pml(C62A/C65A) cells exhibited increased sister-chromatid exchange and chromosome abnormalities.
49 types of Bloom syndrome cells as assessed by sister-chromatid exchange and micronuclei formation assa
50 d telomere shortening, elevation of telomere sister-chromatid exchanges and increased aphidicolin-ind
51 integrated recombination substrate, unequal sister-chromatid exchanges and repair of collapsed repli
52 omycin C (MMC), as measured by cell killing, sister chromatid exchange, and chromosome aberrations.
53 these cells results in chromosome breakage, sister chromatid exchange, and cytotoxicity by a mechani
54 51-mediated D-loop formation, suppression of sister chromatid exchange, and resistance to camptotheci
55 ases karyotype abnormalities and spontaneous sister chromatid exchange, and slows down cell prolifera
56 tability, as quantified by chromatid breaks, sister chromatid exchanges, and H2AX phosphorylation.
57 quency of recombination, gene amplification, sister chromatid exchanges, and micronuclei formation in
58 come hypermutable, exhibit high frequency of sister chromatid exchanges, and show increased micronucl
59 lts may explain why cytologically observable sister chromatid exchanges are induced only weakly by DN
60 fects, including specific gene mutations and sister chromatid exchanges, are induced in neighboring,
61 we examined these cell types for evidence of sister chromatid exchange at telomeres, and observed an
62 centromeric CO-FISH patterns consistent with sister chromatid exchange at the frequency of 5% in prim
65 BLM, telomeric circle formation and telomere sister chromatid exchange, both arising out of nucleolyt
66 n resistance and increased cisplatin-induced sister chromatid exchange, both of which were reversed b
67 s expressing BLM-S144A show normal levels of sister chromatid exchange but fail to maintain the mitot
68 We previously found that the induction of sister chromatid exchanges by UV irradiation was greatly
69 s to telomere shortening, elevated telomeric sister chromatid exchanges, C-circle formation as well a
70 nomic instability and increased frequency of sister chromatid exchange characteristic of Bloom's synd
71 ly 7-methylguanine), can specifically induce sister chromatid exchange, chromatid and chromosome gaps
73 relation between chromosomal instability and sister chromatid exchange, delayed mutation, and mismatc
76 eletion of mRtel1 increased the frequency of sister chromatid exchange events and suppressed gene rep
77 ally, evidence of gene conversion or unequal sister chromatid exchange events in T. quasimodo and T.
80 heir integrity, it also permits rare unequal sister chromatid-exchange events within palindromes that
84 e not affected by the absence of Rad51d, but sister chromatid exchange frequencies did fail to be ind
88 d points such as chromosome destabilization, sister chromatid exchanges, gene mutation and amplificat
89 of principle, we show our ability to detect sister chromatid exchanges, genome compartmentalization,
90 d Strand-seq data, to enable fine-mapping of sister chromatid exchanges, germline inversion and to su
91 on can be induced display elevated levels of sister chromatid exchange, gross chromosomal aberrations
92 s can occur by replication slippage, unequal sister chromatid exchange, homologous recombination, and
93 the elevated level of gene targeting and of sister chromatid exchanges, implying that Blm primarily
97 fic biomarkers (DNA and albumin adducts) and sister chromatid exchanges in the blood of 48 reinforced
100 ents are the probable consequence of unequal sister chromatid exchanges involving chromosome 2, as we
101 de the evidence that NRSS, following unequal sister chromatid exchange, is a mechanism by which GSCs
102 e show that gene conversion, and not unequal sister chromatid exchange, is the predominant recombinat
103 hey suggest that gene conversion rather than sister chromatid exchange may be the primary recombinati
105 BS cells, chromosomal abnormalities such as sister chromatid exchanges occur at highly elevated rate
106 orce in the evolution of the rRNA genes with sister chromatid exchange occurring more often than exch
108 with RAD18 deficiency, reverses the elevated sister chromatid exchange of the rad18 mutant, and reduc
111 ut R1 and R2 retrotransposition the frequent sister chromatid exchanges postulated from various empir
112 , SWS1-SWSAP1-SPIDR drives the high level of sister-chromatid exchange, promotes long-range loss of h
113 nce of chromosomal gaps and breaks, elevated sister chromatid exchange, quadriradial formations, and
114 re unstable genetically and exhibit frequent sister chromatid exchanges, reflective of homologous rec
115 cause in its absence cells display increased sister chromatid exchanges, replication origin firing an
116 ir at endogenous genomic loci by combining a sister chromatid exchange (SCE) assay with fluorescent i
118 , called Strand-seq, that can be used to map sister chromatid exchange (SCE) events genome-wide in si
119 This activity suppresses potentially harmful sister chromatid exchange (SCE) events in wild-type cell
120 ay be responsible for the elevated levels of sister chromatid exchange (SCE) found in BLM(-/-) cells.
122 d human aging, we analyzed the dependence of sister chromatid exchange (SCE) frequencies on location
124 p53 further enhanced the rate of spontaneous sister chromatid exchange (SCE) in Bloom syndrome (BS) c
127 likely to be accommodated by adjustments in sister chromatid exchange (SCE) rate, rather than by dir
128 mportance of G2 arrest in DNA damage-induced sister chromatid exchange (SCE) was evident by a 10-fold
129 recombination visualized cytogenetically as sister chromatid exchange (SCE), and that this rate is d
131 the simultaneous high-resolution mapping of sister chromatid exchange (SCE), facilitating the study
132 , 10- and 30-fold higher rate of spontaneous sister chromatid exchange (SCE), heteroallelic recombina
134 n a significant increase in the frequency of sister chromatid exchange (SCE), whereas deleting both B
135 DT40 cells results in an increased level of sister chromatid exchange (SCE)--the hallmark feature of
140 mic instability epitomized by high levels of sister-chromatid exchange (SCE) and cancer predispositio
141 ctures in vivo, increase spontaneous unequal sister-chromatid exchange (SCE) in vegetatively growing
143 der characterized cellularly by increases in sister chromatid exchanges (SCEs) and numbers of micronu
144 defective for BLM exhibit elevated levels of sister chromatid exchanges (SCEs) and patients with Bloo
147 al results found an increased association of sister chromatid exchanges (SCEs) at PATRR regions in ex
148 x2(null) cells exhibited reduced spontaneous sister chromatid exchanges (SCEs) but this was not due t
149 itization with caffeine and the induction of sister chromatid exchanges (SCEs) by UV irradiation are
150 suggestion that inter-sister crossovers, or sister chromatid exchanges (SCEs), are quite common.(2-1
151 somal instability, characterized by elevated sister chromatid exchanges (SCEs), as well as chromosoma
152 isiae RAD51 in DNA damage-associated unequal sister chromatid exchanges (SCEs), translocations, and i
153 repair of mitomycin C (MMC)-induced DSBs and sister chromatid exchanges (SCEs), two RAD51-dependent p
156 eted of BLAP75 display an increased level of sister-chromatid exchange, similar to cells depleted of
157 telomeres may be maintained through telomere sister chromatid exchange (T-SCE) in murine telomere rev
158 elicase-deficient mutant, abolished telomere sister chromatid exchange (T-SCE), indicating that WRN n
159 cytic leukemia (PML) bodies (APBs), telomere sister chromatid exchanges (T-SCEs), and extrachromosoma
161 ophila melanogaster, which relies on unequal sister chromatid exchange (USCE) initiated by DNA breaks
162 of BS and FA cells-an elevated frequency of sister chromatid exchanges-was due to a loss of interact
165 subjects, albumin and DNA adducts as well as sister chromatid exchanges were significantly correlated
168 inery, and increases C-circles and telomeric sister chromatid exchanges, without increasing telomeric